A Facilitatory Effect of Perceptual Incongruity on Target-Source Matching in Pictorial Metaphors of Chinese Advertising: EEG Evidence

After having been told they were free to accept or refuse, pupils aged 6–7 and 10–11 (tested individually) were led to agree to taste a soup that looked disgusting (phase 1: initial counter-motivational obligation). Before tasting the soup, they had to state what they thought about it. A week later, they were asked whether they wanted to try out some new needles that had supposedly been invented to make vaccinations less painful. Agreement or refusal to try was noted, along with the size of the needle chosen in case of agreement (phase 2: act generalization). The main findings included (1) a strong dissonance reduction effect in phase 1, especially for the younger children (rationalization), (2) a generalization effect in phase 2 (foot-in-the-door effect), and (3) a facilitatory effect on generalization of internal causal explanations about the initial agreement. The results are discussed in relation to the distinction between rationalization and internalization.

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Aluminum Suppresses Effect of Nicotine on Gamma Oscillations (20-40 Hz) in Mouse Hippocampal Slices

CNS & Neurological Disorders - Drug Targets ◽

10.2174/1871527317666180619155644 ◽

2018 ◽

Vol 17 (6) ◽

pp. 404-411 ◽

Cited By ~ 4

Author(s):

Syeda Mehpara Farhat ◽

Touqeer Ahmed

Keyword(s):

Nicotinic Acetylcholine Receptors ◽

Cholinergic System ◽

Acetylcholine Receptors ◽

Peak Power ◽

Hippocampal Slices ◽

Field Potential ◽

Gamma Oscillations ◽

Gamma Oscillation ◽

Facilitatory Effect

Background: Aluminum (Al) causes neurodegeneration and its toxic effects on cholinergic system in the brain is well documented. However, it is unknown whether and how Al changes oscillation patterns, driven by the cholinergic system, in the hippocampus. Objective: We studied acute effects of Al on nicotinic acetylcholine receptors (nAChRs)-mediated modulation of persistent gamma oscillations in the hippocampus. Method: The field potential recording was done in CA3 area of acute hippocampal slices. Results: Carbachol-induced gamma oscillation peak power increased (1.32±0.09mV2/Hz, P<0.01) in control conditions (without Al) by application of 10µM nicotine as compared to baseline value normalized to 1. This nicotine-induced facilitation of gamma oscillation peak power was found to depend on non-α7 nAChRs. In slices with Al pre-incubation for three to four hours, gamma oscillation peak power was reduced (5.4±1.8mV2/Hz, P<0.05) and facilitatory effect of nicotine on gamma oscillation peak power was blocked as compared to the control (18.06±2.1mV2/Hz) or one hour Al pre-incubated slices (11.3±2.5mV2/Hz). Intriguingly wash-out, after three to four hours of Al incubation, failed to restore baseline oscillation power and its facilitation by nicotine as no difference was observed in gamma oscillation peak power between Al wash-out slices (3.4±1.1mV2/Hz) and slices without washout (3.6±0.9mV2/Hz). Conclusion: This study shows that at cellular level, exposure of hippocampal tissue to Al compromised nAChR-mediated facilitation of cholinergic hippocampal gamma oscillations. Longer in vitro Al exposure caused permanent changes in hippocampal oscillogenic circuitry and changed its sensitivity to nAChR-modulation. This study will help to understand the possible mechanism of cognitive decline induced by Al.

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Subcortical circuits mediate communication between primary sensory cortical areas in mice

Nature Communications ◽

10.1038/s41467-021-24200-x ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Michael Lohse ◽

Johannes C. Dahmen ◽

Victoria M. Bajo ◽

Andrew J. King

Keyword(s):

Cortical Neurons ◽

Common Property ◽

Primary Auditory Cortex ◽

Facilitatory Effect ◽

Thalamic Nuclei ◽

Auditory Midbrain ◽

Cortical Areas ◽

Auditory Responses ◽

Evoked Activity

AbstractIntegration of information across the senses is critical for perception and is a common property of neurons in the cerebral cortex, where it is thought to arise primarily from corticocortical connections. Much less is known about the role of subcortical circuits in shaping the multisensory properties of cortical neurons. We show that stimulation of the whiskers causes widespread suppression of sound-evoked activity in mouse primary auditory cortex (A1). This suppression depends on the primary somatosensory cortex (S1), and is implemented through a descending circuit that links S1, via the auditory midbrain, with thalamic neurons that project to A1. Furthermore, a direct pathway from S1 has a facilitatory effect on auditory responses in higher-order thalamic nuclei that project to other brain areas. Crossmodal corticofugal projections to the auditory midbrain and thalamus therefore play a pivotal role in integrating multisensory signals and in enabling communication between different sensory cortical areas.

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Phrase Table Combination Based on Symmetrization of Word Alignment for Low-Resource Languages

Applied Sciences ◽

10.3390/app11041868 ◽

2021 ◽

Vol 11 (4) ◽

pp. 1868

Author(s):

Sari Dewi Budiwati ◽

Al Hafiz Akbar Maulana Siagian ◽

Tirana Noor Fatyanosa ◽

Masayoshi Aritsugi

Keyword(s):

Language Model ◽

Word Alignment ◽

Low Resource ◽

Relative Improvement ◽

Direct Translation ◽

The Common ◽

Target Source

Phrase table combination in pivot approaches can be an effective method to deal with low-resource language pairs. The common practice to generate phrase tables in pivot approaches is to use standard symmetrization, i.e., grow-diag-final-and. Although some researchers found that the use of non-standard symmetrization could improve bilingual evaluation understudy (BLEU) scores, the use of non-standard symmetrization has not been commonly employed in pivot approaches. In this study, we propose a strategy that uses the non-standard symmetrization of word alignment in phrase table combination. The appropriate symmetrization is selected based on the highest BLEU scores in each direct translation of source–target, source–pivot, and pivot–target of Kazakh–English (Kk–En) and Japanese–Indonesian (Ja–Id). Our experiments show that our proposed strategy outperforms the direct translation in Kk–En with absolute improvements of 0.35 (a 11.3% relative improvement) and 0.22 (a 6.4% relative improvement) BLEU points for 3-gram and 5-gram, respectively. The proposed strategy shows an absolute gain of up to 0.11 (a 0.9% relative improvement) BLEU points compared to direct translation for 3-gram in Ja–Id. Our proposed strategy using a small phrase table obtains better BLEU scores than a strategy using a large phrase table. The size of the target monolingual and feature function weight of the language model (LM) could reduce perplexity scores.

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Monitoring of the plasma generated by a gas-puff target source

Physical Review Accelerators and Beams ◽

10.1103/physrevaccelbeams.22.052901 ◽

2019 ◽

Vol 22 (5) ◽

Cited By ~ 2

Author(s):

A. Torrisi ◽

P. W. Wachulak ◽

H. Fiedorowicz ◽

L. Torrisi

Keyword(s):

Target Source

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Serotonin-reinstatement of luteinizing hormone surges after loss of positive feedback in ovariectomized rats bearing subcutaneous capsules containing oestrogen

Journal of Endocrinology ◽

10.1677/joe.0.0980007 ◽

1983 ◽

Vol 98 (1) ◽

pp. 7-17 ◽

Cited By ~ 3

Author(s):

R. F. Walker

Keyword(s):

Positive Feedback ◽

Ovariectomized Rats ◽

Facilitatory Effect ◽

Serum Progesterone ◽

Serotonin Content ◽

Serum Lh ◽

Serotonin Turnover ◽

Lh Rh ◽

Lh Releasing Hormone ◽

Feedback Responses

In ovariectomized rats treated chronically with oestrogen there is a loss of positive feedback effects on LH secretion. This was not due to depletion of pituitary LH since injection of LH releasing hormone (LH-RH; 50 ng/100 g body wt) caused a significant (P < 0·01) rise in serum LH even after the loss of spontaneous LH surges. However, the magnitude of the increase in serum LH in response to LH-RH was greater (412 ± 41 μg/l) before than after (291 ± 29 μg/l) loss of the LH surges. Excessive blood sampling was also not responsible, since positive feedback responses declined comparably in rats bled daily or once every 3–4 days. Progesterone (0·5 mg s.c.), administered for 5 consecutive days, failed to restore LH surges indicating that deficiency of this steroid after ovariectomy does not cause positive feedback responses to disappear in rats exposed chronically to oestrogen. Moreover regular daily fluctuations in serum progesterone, probably of adrenal origin, occurred before as well as after daily LH surges were lost. Serotonin content and turnover were depressed (P < 0·05) when ovariectomized rats first received the subcutaneous capsules containing oestrogen. This change correlated temporally with the onset of daily LH surges and was eventually lost. After 30 days exposure to oestrogen, serotonin turnover increased (P < 0·01) and positive feedback responses were absent. Catecholamine levels and turnover did not show differential responses to oestrogen and were depressed after acute as well as chronic steroid treatment. p-Chlorophenylalanine (pCPA; 250 mg/kg)+ l-dihydroxyphenylalanine (l-DOPA; 200 mg/kg), which depress serotonin and enhance catecholamine synthesis respectively, failed to reinstate LH surges, but these were restored in 22% of the rats receiving l-DOPA alone. pCPA, followed 2 days later by 5-hydroxytryptophan (5-HTP) at 11.00 h, reinstated LH surges in 88% of rats, and a dose–response curve showed that as little as 4 mg 5-HTP/kg stimulated repetitive LH surges when given with pCPA according to this schedule. However, the administration of α-methyl-p-tyrosine + l-DOPA, an analogous treatment involving catecholamines, was only marginally effective (15%). These findings suggest that perturbations of monoamine metabolism occurring in ovariectomized rats exposed to oestrogen for several weeks contribute to loss of daily LH surges. Since pCPA + 5-HTP restored LH surges most effectively, then positive feedback may disappear as the facilitatory effect of serotonin is lost after chronic oestrogen administration.

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Nicotine paradoxically affects the facilitatory effect of ovarian hormones on the adenosine receptor-mediated renal vasodilation

European Journal of Pharmacology ◽

10.1016/j.ejphar.2013.04.011 ◽

2013 ◽

Vol 710 (1-3) ◽

pp. 1-9 ◽

Cited By ~ 4

Author(s):

Eman Y. Gohar ◽

Sahar M. El-gowilly ◽

Hanan M. El-Gowelli ◽

Mahmoud M. El-Mas

Keyword(s):

Adenosine Receptor ◽

Ovarian Hormones ◽

Facilitatory Effect

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Neural network dysfunction in bipolar depression: clues from the efficacy of lamotrigine

Biochemical Society Transactions ◽

10.1042/bst0371080 ◽

2009 ◽

Vol 37 (5) ◽

pp. 1080-1084 ◽

Cited By ~ 12

Author(s):

Charles H. Large ◽

Elena Di Daniel ◽

Xingbao Li ◽

Mark S. George

Keyword(s):

Bipolar Disorder ◽

Valproic Acid ◽

Protein Kinase ◽

Glycogen Synthase ◽

Bipolar Depression ◽

Inhibitory Effect ◽

Mood Stabilizers ◽

Mitogen Activated Protein Kinase ◽

Facilitatory Effect

One strategy to understand bipolar disorder is to study the mechanism of action of mood-stabilizing drugs, such as valproic acid and lithium. This approach has implicated a number of intracellular signalling elements, such as GSK3β (glycogen synthase kinase 3β), ERK (extracellular-signal-regulated kinase)/MAPK (mitogen-activated protein kinase) or protein kinase C. However, lamotrigine does not seem to modulate any of these targets, which is intriguing given that its profile in the clinic differs from that of valproic acid or lithium, with greater efficacy to prevent episodes of depression than mania. The primary target of lamotrigine is the voltage-gated sodium channel, but it is unclear why inhibition of these channels might confer antidepressant efficacy. In healthy volunteers, we found that lamotrigine had a facilitatory effect on the BOLD (blood-oxygen-level-dependent) response to TMS (transcranial magnetic stimulation) of the prefrontal cortex. This effect was in contrast with an inhibitory effect of lamotrigine when TMS was applied over the motor cortex. In a follow-up study, a similar prefrontal specific facilitatory effect was observed in a larger cohort of healthy subjects, whereas valproic acid inhibited motor and prefrontal cortical TMS-induced BOLD response. In vitro, we found that lamotrigine (3–10 μM) enhanced the power of gamma frequency network oscillations induced by kainic acid in the rat hippocampus, an effect that was not observed with valproic acid (100 μM). These data suggest that lamotrigine has a positive effect on corticolimbic network function that may differentiate it from other mood stabilizers. The results are also consistent with the notion of corticolimbic network dysfunction in bipolar disorder.

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High environmental salinity induces memory enhancement and increases levels of brain angiotensin-like peptides in the crab Chasmagnathus granulatus

Journal of Experimental Biology ◽

10.1242/jeb.203.22.3369 ◽

2000 ◽

Vol 203 (22) ◽

pp. 3369-3379 ◽

Cited By ~ 1

Author(s):

A. Delorenzi ◽

B. Dimant ◽

L. Frenkel ◽

V.E. Nahmod ◽

D.R. Nassel ◽

...

Keyword(s):

Angiotensin Ii ◽

Brackish Water ◽

Sea Water ◽

Immunohistochemical Analysis ◽

Facilitatory Effect ◽

Long Term Memory ◽

Stimulus Context ◽

Memory Enhancement ◽

Chasmagnathus Granulatus

Previous work on the brackish-water crab Chasmagnathus granulatus demonstrated that an endogenous peptide similar to angiotensin II plays a significant role in enhancing long-term memory that involves an association between context and an iterative danger stimulus (context-signal memory). The present results show that this memory enhancement could be produced by moving crabs from brackish water to sea water (33.0%) and keeping them there for at least 4 days. The possibility that such a facilitatory effect is due to osmotic stress is ruled out. Coincidentally, the level of angiotensin-II-like peptides in crab brain, measured by radioimmunoassay, increases with the length of exposure to sea water, reaching a significantly different level at the fourth day. The presence of angiotensin-II-like immunoreactive material in neural structures of the supraoesophageal and eyestalk ganglia was confirmed by immunohistochemical analysis. The results are interpreted as supporting the hypothesis that exposure to water of high salinity is an external cue triggering a process mediated by angiotensins that leads to enhanced memory in these crabs.

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Activation of Presynaptic Group III Metabotropic Receptors Enhances Glutamate Release in Rat Entorhinal Cortex

Journal of Neurophysiology ◽

10.1152/jn.2000.83.5.2519 ◽

2000 ◽

Vol 83 (5) ◽

pp. 2519-2525 ◽

Cited By ~ 27

Author(s):

D. Ieuan Evans ◽

Roland S. G. Jones ◽

Gavin Woodhall

Keyword(s):

Synaptic Transmission ◽

Entorhinal Cortex ◽

Metabotropic Glutamate Receptors ◽

Glutamate Release ◽

Facilitatory Effect ◽

Metabotropic Receptors ◽

Patch Clamp Technique ◽

Group Iii ◽

Bath Application ◽

Layer V

The role of group III metabotropic glutamate receptors (mGluRs) in modulating excitatory synaptic transmission was investigated in the rat entorhinal cortex (EC) in vitro. AMPA receptor-mediated excitatory postsynaptic currents (EPSCs) were recorded in the whole cell configuration of the patch-clamp technique from visually identified neurons in layers V and II. In layer V, bath application of the specific group III mGluR agonist L(+)-2-amino-4-phosphonobutyric acid (L-AP4, 500 μM) resulted in a marked facilitation of both spontaneous and activity-independent “miniature” (s/mEPSC) event frequency. The facilitatory effect of L-AP4 (100 μM) on sEPSC frequency prevailed in the presence ofdl−2-amino-5-phosphonopentanoic acid (100 μM) but was abolished by the group III antagonist (RS)-cyclopropyl-4-phosphonophenylglycine (20 μM). These data confirmed that group III mGluRs, and not N-methyl-d-aspartate (NMDA) receptors were involved in the response to L-AP4. Bath application of the specific mGluR4a agonist (1S,3R,4S)-1-aminocyclopentane-1,2,4-tricarboxylic acid (20 μM) also had a facilitatory effect on sEPSC frequency, suggesting involvement of mGluR4a. In layer II neurons, L-AP4 caused a reduction in sEPSC frequency but did not affect mEPSCs recorded in the presence of tetrodotoxin. These findings suggest that a group III mGluR with mGluR4a-like pharmacology is involved in modulating synaptic transmission in layer V cells of the EC. The effect on mEPSCs suggests that this receptor is located presynaptically and that its activation results in a direct facilitation of glutamate release. This novel facilitatory effect is specific to layer V and, to our knowledge, is the first report of a direct facilitatory action of group III mGluRs on synaptic transmission. In layer II, L-AP4 had an inhibitory effect on glutamate release similar to that reported in other brain regions.

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